Genetic analysis of the rice jasmonate receptors reveals specialized functions for OsCOI2.

COI1-mediated perception of jasmonate is critical for plant development and responses to environmental stresses. Monocots such as rice have two groups of COI genes due to gene duplication: OsCOI1a and OsCOI1b that are functionally equivalent to the dicotyledons COI1 and OsCOI2 whose function remains unclear. In order to assess the function of OsCOI2 and its functional redundancy with COI1 genes, we developed a series of rice mutants in the 3 genes OsCOI1a, OsCOI1b and OsCOI2 by CRISPR Cas9-mediated editing and characterized their phenotype and responses to jasmonate. Characterization of OsCOI2 uncovered its important roles in root, leaf and flower development. In particular, we show that crown root growth inhibition by jasmonate relies on OsCOI2 and not on OsCOI1a nor on OsCOI1b, revealing a major function for the non-canonical OsCOI2 in jasmonate-dependent control of rice root growth. Collectively, these results point to a specialized function of OsCOI2 in the regulation of plant development in rice and indicate that sub-functionalisation of jasmonate receptors has occurred in the monocot phylum.

The fungal metabolite 4-hydroxyphenylacetic acid from Neofusicoccum parvum modulates defence responses in grapevine.

In a consequence of global warming, grapevine trunk diseases (GTDs) have become a pertinent problem to viticulture, because endophytic fungi can turn necrotrophic upon host stress killing the plant. In Neofusicoccum parvum Bt-67, plant-derived ferulic acid makes the fungus release Fusicoccin aglycone triggering plant cell death. Now, we show that the absence of ferulic acid lets the fungus secrete 4-hydroxyphenylacetic acid (4-HPA), mimicking the effect of auxins on grapevine defence and facilitating fungal spread. Using Vitis suspension cells, we dissected the mode of action of 4-HPA during defence triggered by the bacterial cell-death elicitor, harpin. Early responses (cytoskeletal remodelling and calcium influx) are inhibited, as well as the expression of Stilbene Synthase 27 and phytoalexin accumulation. In contrast to other auxins, 4-HPA quells transcripts for the auxin conjugating GRETCHEN HAGEN 3. We suggest that 4-HPA is a key component of the endophytic phase of N. parvum Bt-67 preventing host cell death. Therefore, our study paves the way to understand how GTDs regulate their latent phase for successful colonisation, before turning necrotrophic and killing the vines.

Jasmonate signaling controls negative and positive effectors of salt stress tolerance in rice.

Plant responses to salt exposure involve large reconfigurations of hormonal pathways that orchestrate physiological changes towards tolerance. Jasmonate (JA) hormones are essential to withstand biotic and abiotic assaults, but their roles in salt tolerance remain unclear. Here we describe the dynamics of JA metabolism and signaling in root and leaf tissue of rice, a plant species that is highly exposed and sensitive to salt. Roots activate the JA pathway in an early pulse, while the second leaf displays a biphasic JA response with peaks at 1 h and 3 d post-exposure. Based on higher salt tolerance of a rice JA-deficient mutant (aoc), we examined, through kinetic transcriptome and physiological analysis, the salt-triggered processes that are under JA control. Profound genotype-differential features emerged that could underlie the observed phenotypes. Abscisic acid (ABA) content and ABA-dependent water deprivation responses were impaired in aoc shoots. Moreover, aoc accumulated more Na+ in roots, and less in leaves, with reduced ion translocation correlating with root derepression of the HAK4 Na+ transporter gene. Distinct reactive oxygen species scavengers were also stronger in aoc leaves, along with reduced senescence and chlorophyll catabolism markers. Collectively, our results identify contrasted contributions of JA signaling to different sectors of the salt stress response in rice.

Chitosan triggers actin remodelling and activation of defence genes that is repressed by calcium influx in grapevine cells.

Defence to pathogens must be specific. In the past, we have dissected early signalling deployed by bacterial elicitors in a grapevine cell system. In the current work, we asked, how defence of fungi differs. Fungal diseases of grapevine pose great challenges for global viticulture and require massive plant protection measures. Plant cells are able to sense chitin, a central component of fungal cell walls and respond by activation of basal defence. We, therefore mapped early defence responses evoked by chitosan, a chitin fragment able to bind to chitin receptors. We found an activation of calcium influx, monitored by extracellular alkalinisation due to a co-transport of protons, remodelling of actin (but not of microtubules), and the activation of transcripts for phytoalexin synthesis, jasmonate-signalling, salicylate signalling, and chitinase. Interestingly, Gadolinium, an inhibitor of calcium influx, can inhibit extracellular alkalinisation in response to chitosan, while the induction of the phytoalexin synthesis transcripts was specifically promoted. In contrast, both DMSO and benzyl alcohol, compounds known to modulate membrane fluidity, partially inhibited the transcript responses to chitosan. We discuss these data with a model, where chitosan deploys signalling culminating in activation of defence related transcripts, but at the same time activates calcium influx that negatively feeds back on the same signal chain, which might be a mechanism to achieve a temporal signature that is rapid, but transient.

Plant defense under Arctic light conditions: Can plants withstand invading pests?

Global warming is predicted to change the growth conditions for plants and crops in regions at high latitudes (>60° N), including the Arctic. This will be accompanied by alterations in the composition of natural plant and pest communities, as herbivorous arthropods will invade these regions as well. Interactions between previously non-overlapping species may occur and cause new challenges to herbivore attack. However, plants growing at high latitudes experience less herbivory compared to plants grown at lower latitudes. We hypothesize that this finding is due to a gradient of constitutive chemical defense towards the Northern regions. We further hypothesize that higher level of defensive compounds is mediated by higher level of the defense-related phytohormone jasmonate. Because its biosynthesis is light dependent, Arctic summer day light conditions can promote jasmonate accumulation and, hence, downstream physiological responses. A pilot study with bilberry (Vaccinium myrtillus) plants grown under different light regimes supports the hypothesis.

Jasmonic acid contributes to rice resistance against Magnaporthe oryzae.

BACKGROUND: The annual yield losses caused by the Rice Blast Fungus, Magnaporthe oryzae, range to the equivalent for feeding 60 million people. To ward off infection by this fungus, rice has evolved a generic basal immunity (so called compatible interaction), which acts in concert with strain-specific defence (so-called incompatible interaction). The plant-defence hormone jasmonic acid (JA) promotes the resistance to M. oryzae, but the underlying mechanisms remain elusive. To get more insight into this open question, we employ the JA-deficient mutants, cpm2 and hebiba, and dissect the JA-dependent defence signalling in rice for both, compatible and incompatible interactions. RESULTS: We observe that both JA-deficient mutants are more susceptible to M. oryzae as compared to their wild-type background, which holds true for both types of interactions as verified by cytological staining. Secondly, we observe that transcripts for JA biosynthesis (OsAOS2 and OsOPR7), JA signalling (OsJAZ8, OsJAZ9, OsJAZ11 and OsJAZ13), JA-dependent phytoalexin synthesis (OsNOMT), and JA-regulated defence-related genes, such as OsBBTI2 and OsPR1a, accumulate after fungal infection in a pattern that correlates with the amplitude of resistance. Thirdly, induction of defence transcripts is weaker during compatible interaction. CONCLUSION: The study demonstrates the pivotal role of JA in basal immunity of rice in the resistance to M. oryzae in both, compatible and incompatible interactions.

Gain time to adapt: How sorghum acquires tolerance to salinity.

Salinity is a global environmental threat to agricultural production and food security around the world. To delineate salt-induced damage from adaption events we analysed a pair of sorghum genotypes which are contrasting in their response to salt stress with respect to physiological, cellular, metabolomic, and transcriptional responses. We find that the salt-tolerant genotype Della can delay the transfer of sodium from the root to the shoot, more swiftly deploy accumulation of proline and antioxidants in the leaves and transfer more sucrose to the root as compared to its susceptible counterpart Razinieh. Instead Razinieh shows metabolic indicators for a higher extent photorespiration under salt stress. Following sodium accumulation by a fluorescent dye in the different regions of the root, we find that Della can sequester sodium in the vacuoles of the distal elongation zone. The timing of the adaptive responses in Della leaves indicates a rapid systemic signal from the roots that is travelling faster than sodium itself. We arrive at a model where resistance and susceptibility are mainly a matter of temporal patterns in signalling.

Cold-Induced Nuclear Import of CBF4 Regulates Freezing Tolerance.

C-repeat binding factors (CBFs) are crucial transcriptional activators in plant responses to low temperature. CBF4 differs in its slower, but more persistent regulation and its role in cold acclimation. Cold acclimation has accentuated relevance for tolerance to late spring frosts as they have become progressively more common, as a consequence of blurred seasonality in the context of global climate change. In the current study, we explore the functions of CBF4 from grapevine, VvCBF4. Overexpression of VvCBF4 fused to GFP in tobacco BY-2 cells confers cold tolerance. Furthermore, this protein shuttles from the cytoplasm to the nucleus in response to cold stress, associated with an accumulation of transcripts for other CBFs and the cold responsive gene, ERD10d. This response differs for chilling as compared to freezing and is regulated differently by upstream signalling involving oxidative burst, proteasome activity and jasmonate synthesis. The difference between chilling and freezing is also seen in the regulation of the CBF4 transcript in leaves from different grapevines differing in their cold tolerance. Therefore, we propose the quality of cold stress is transduced by different upstream signals regulating nuclear import and, thus, the transcriptional activation of grapevine CBF4.

The fungal elicitor eutypine from Eutypa lata activates basal immunity through its phenolic side chains.

Grapevine trunk diseases (GTDs) affect grape production and reduce vineyard longevity worldwide. Since the causative fungi also occur in asymptomatic trunks, we address disease outbreak in terms of altered chemical communication between host and endophyte. Here, we identified four chemically similar secondary metabolites secreted by the GTD-associated fungus Eutypa lata to analyse their modes of action in a grapevine cell culture of Vitis rupestris, where microtubules were tagged by GFP. Treatment with the metabolite eutypine activated defence responses, evident from extracellular alkalinisation and induction of defence genes. Eutypinol, instead, eliminated microtubules, in contrast to the other three compounds. Furthermore, we evaluated the effect of four corresponding chemical analogues of these compounds, sharing the phenolic but lacking the alkyne moiety. These analogues were able to induce similar defence responses in V. rupestris cells, albeit at reduced amplitude. Since closely related moieties differing only in details of the side groups at the phenolic ring differ significantly with respect to the response of the host cell, we propose that these fungal compounds act through a specific binding site at the membrane of grapevine cells. We corroborate this specificity by combination experiments, where the eutypine and the eutypinol analogues behave competitively with respect to the elicited responses. In summary, Eutypa lata secretes compounds that elicit host defence in a specific manner by interfering with early events of immunity signalling. This supports the notion that a real understanding of GTDs has to address inter-organismic chemical communication.

The Minus-End-Directed Kinesin OsDLK Shuttles to the Nucleus and Modulates the Expression of Cold-Box Factor 4.

The transition to terrestrial plants was accompanied by a progressive loss of microtubule minus-end-directed dynein motors. Instead, the minus-end-directed class-XIV kinesins expanded considerably, likely related to novel functions. One of these motors, OsDLK (Dual Localisation Kinesin from rice), decorates cortical microtubules but moves into the nucleus in response to cold stress. This analysis of loss-of-function mutants in rice indicates that OsDLK participates in cell elongation during development. Since OsDLK harbours both a nuclear localisation signal and a putative leucin zipper, we asked whether the cold-induced import of OsDLK into the nucleus might correlate with specific DNA binding. Conducting a DPI-ELISA screen with recombinant OsDLKT (lacking the motor domain), we identified the Opaque2 motif as the most promising candidate. This motif is present in the promoter of NtAvr9/Cf9, the tobacco homologue of Cold-Box Factor 4, a transcription factor involved in cold adaptation. A comparative study revealed that the cold-induced accumulation of NtAvr9/Cfp9 was specifically quelled in transgenic BY-2 cells overexpressing OsDLK-GFP. These findings are discussed as a working model, where, in response to cold stress, OsDLK partitions from cortical microtubules at the plasma membrane into the nucleus and specifically modulates the expression of genes involved in cold adaptation.

A rice tubulin tyrosine ligase like 12 regulates phospholipase D activity and tubulin synthesis.

All plant α-tubulins encode a C-terminal tyrosine. An elusive tubulin tyrosine carboxypeptidase can cleave off, and a tubulin tyrosine ligase (TTL) re-ligate this tyrosine. The biological function of this cycle remains unclear but may correlate with microtubule stability. To get insight into the functional context of this phenomenon, we used cold-induced elimination of microtubules as experimental model. In previous work, we had analysed a rice TTL-like 12 (OsTTLL12), the only potential candidate of plant TTL. To follow the effect of OsTTLL12 upon microtubule responses in vivo, we expressed OsTTLL12-RFP into tobacco BY-2 cells stably overexpressing NtTUA3-GFP. We found that overexpression of OsTTLL12-RFP made microtubules disappear faster in response to cold stress, accompanied with more rapid Ca2+ influx, culminating in reduced cold tolerance. Treatment with different butanols indicated that α-tubulin detyrosination/tyrosination differently interacts with phospholipase D (PLD) dependent signalling. In fact, rice PLDα1 decorated microtubules and increased detyrosinated α-tubulin. Unexpectedly, overexpression of the two proteins (OsTTLL12-RFP, NtTUA3-GFP) mutually regulated the accumulation of their transcripts, leading us to a model, where tubulin detyrosination feeds back upon tubulin transcripts and defines a subset of microtubules for interaction with PLD dependent stress signalling.

The jasmonate biosynthesis Gene OsOPR7 can mitigate salinity induced mitochondrial oxidative stress.

Salinity poses a serious threat to global agriculture and human food security. A better understanding of plant adaptation to salt stress is, therefore, mandatory. In the non-photosynthetic cells of the root, salinity perturbs oxidative balance in mitochondria, leading to cell death. In parallel, plastids accumulate the jasmonate precursor cis (+)12-Oxo-Phyto-Dienoic Acid (OPDA) that is then translocated to peroxisomes and has been identified as promoting factor for salt-induced cell death as well. In the current study, we probed for a potential interaction between these three organelles that are primarily dealing with oxidative metabolism. We made use of two tools: (i) Rice OPDA Reductase 7 (OsOPR7), an enzyme localised in peroxisomes converting OPDA into the precursors of the stress hormone JA-Ile. (ii) A Trojan Peptoid, Plant PeptoQ, which can specifically target to mitochondria and scavenge excessive superoxide accumulating in response to salt stress. We show that overexpression of OsOPR7 as GFP fusion in tobacco (Nicotiana tabacum L. cv. Bright Yellow 2, BY-2) cells, as well as a pretreatment with Plant PeptoQ can mitigate salt stress with respect to numerous aspects including proliferation, expansion, ionic balance, redox homeostasis, and mortality. This mitigation correlates with a more robust oxidative balance, evident from a higher activity of superoxide dismutase (SOD), lower levels of superoxide and lipid peroxidation damage, and a conspicuous and specific upregulation of mitochondrial SOD transcripts. Although both, Plant PeptoQ and ectopic OsOPR7, were acting in parallel and mostly additive, there are two specific differences: (i) OsOPR7 is strictly localised to the peroxisomes, while Plant PeptoQ found in mitochondria. (ii) Plant PeptoQ activates transcripts of NAC, a factor involved in retrograde signalling from mitochondria to the nucleus, while these transcripts are suppressed significantly in the cells overexpressing OsOPR7. The fact that overexpression of a peroxisomal enzyme shifting the jasmonate pathway from the cell-death signal OPDA towards JA-Ile, a hormone linked with salt adaptation, is accompanied by more robust redox homeostasis in a different organelle, the mitochondrion, indicates that cross-talk between peroxisome and mitochondrion is a crucial factor for efficient adaptation to salt stress.

Aluminum can activate grapevine defense through actin remodeling.

In the current study, we used a grapevine cell line in which actin filaments are labeled by GFP to show that aluminum causes actin remodeling through activation of NADPH oxidase in the plasma membrane, followed by activation of phytoalexin synthesis genes. Elimination of actin filaments by latrunculin B disrupts gene activation and inhibition of MAPK signaling by the inhibitor PD98059. Interestingly, aluminum also induces the transcription of ISOCHORISMATE SYNTHASE, a key enzyme for the synthesis of salicylic acid, as well as PR1, a gene that is known to be responsive to salicylic acid. However, while salicylic acid responses are usually a hallmark of the hypersensitive response, aluminum-triggered defense is not accompanied by cell death. Both actin remodeling and gene activation in response to aluminum can be suppressed by the natural auxin indole acetic acid, suggesting that the actin response is not caused by nonspecific signaling. Further evidence for the specificity of the aluminum-triggered activation of phytoalexin synthesis genes comes from experiments in which plant peptide elicitors induce significant cellular mortality but do not evoke induction of these transcription. The response in grapevine cells can be recapitulated in grapevine leaf discs from two genotypes contrasting in stilbene inducibility. Here, aluminum can induce accumulation of the central grapevine phytoalexin, the stilbene aglycone trans-resveratrol; this is preceded by a rapid induction of transcription for RESVERATROL SYNTHASE and the regulating transcription factor MYB14. The amplitude of this induction reflects the general stilbene inducibility of these genotypes, indicating that the aluminum effect is not caused by nonspecific toxicity but by activation of specific signaling pathways. The findings are discussed in relation to a model in which actin filaments activate a specific branch of defense signaling, acting in concert with calcium-dependent PAMP-triggered immunity. This pathway links the apoplastic oxidative burst through MAPK signaling with the activation of defense-related transcription.

Dissecting the membrane-microtubule sensor in grapevine defence.

Specific populations of plant microtubules cooperate with the plasma membrane to sense and process abiotic stress signals, such as cold stress. The current study derived from the question, to what extent this perception system is active in biotic stress signalling. The experimental system consisted of grapevine cell lines, where microtubules or actin filaments are visualised by GFP, such that their response became visible in vivo. We used the bacterial elicitors harpin (inducing cell-death related defence), or flg22 (inducing basal immunity) in combination with modulators of membrane fluidity, or microtubules. We show that DMSO, a membrane rigidifier, can cause microtubule bundling and trigger defence responses, including activation of phytoalexin transcripts. However, DMSO inhibited the gene expression in response to harpin, while promoting the gene expression in response to flg22. Treatment with DMSO also rendered microtubules more persistent to harpin. Paradoxically, Benzylalcohol (BA), a membrane fluidiser, acted in the same way as DMSO. Neither GdCl3, nor diphenylene iodonium were able to block the inhibitory effect of membrane rigidification on harpin-induced gene expression. Treatment with taxol stabilised microtubule against harpin but amplified the response of PAL transcripts. Therefore, the data support implications of a model that deploys specific responses to pathogen-derived signals.

Phytochrome A and its Functional Manifestations in Etiolated and Far-red Light-grown Seedlings of the Wild-type Rice and its Hebiba and Cpm2 Mutants Deficient in the Defense-related Phytohormone Jasmonic Acid.

Interaction between phytochromes and hormones is becoming one of the major issues in plant photophysiology. In this work, effects of defense-related jasmonic acid (JA) on phytochrome A (phyA) were investigated by fluorescence spectroscopy making use of two JA biosynthesis mutants of rice: cpm2 with the inactivated gene allene oxide cyclase and hebiba with additional genes deleted. Constant far-red light (FRc) mediated by phyA reduced its content in the wild type (WT) and mutants, and brought about domination of its light-stable pool (phyA″) in WT and light-labile pool (phyA') in the mutants. Pulsed FRp was much less effective. This FR effect classifies as primarily HIR with a low fluence threshold; it comprises inhibition of phyA biosynthesis, stimulation of phyA″→phyA' transformation and phyA' destruction. In the mutants, phyA suppresses [Pchlide] under FRp (VLFR) and stimulates it under FRc (HIR); these effects are lacking in WT. Similarly, phyA suppresses roots'growth under FRp in the mutants but not in WT. These JA mutant features suggest that JA reduces the phyA functional activity primarily in its phyA″ form mediating HIR. This modulating JA action on phyA functions under FR limiting their extreme manifestations may have contributed to the evolutionary advances of the land plants.

Ancestral chemotypes of cultivated grapevine with resistance to Botryosphaeriaceae-related dieback allocate metabolism towards bioactive stilbenes.

Grapevine trunk diseases have devastating consequences on vineyards worldwide. European wild grapevines (Vitis vinifera subs. sylvestris) from the last viable population in Germany along the Rhine river showed variable degrees of resistance against Neofusicoccum parvum (strain Bt-67), a fungus associated with Botryosphaeriaceae-related dieback. Representative genotypes from different subclades of this population were mapped with respect to their ability to induce wood necrosis, as well as their defence responses in a controlled inoculation system. The difference in colonization patterns could be confirmed by cryo-scanning electron microscopy, while there was no relationship between vessel diameter and infection success. Resistant lines accumulated more stilbenes, that were in addition significantly partitioned to nonglycosylated viniferin trimers. By contrast, the susceptible genotypes accumulated less stilbenes with a significantly higher proportion of glycosylated piceid. We suggest a model in which in the resistant genotypes phenylpropanoid metabolism is channelled rapidly and specifically to the bioactive stilbenes. Our study specifies a resistant chemotype against grapevines trunk diseases and paves a way to breed for resistance against grapevine Botryosphaeriaceae-related dieback.

A rice tubulin tyrosine ligase-like 12 protein affects the dynamic and orientation of microtubules.

The detyrosination/retyrosination cycle is the most common post-translational modification of α-tubulin. Removal of the conserved C-terminal tyrosine of α-tubulin by a still elusive tubulin tyrosine carboxypeptidase, and religation of this tyrosine by a tubulin tyrosine ligase (TTL), are probably common to all eukaryotes. Interestingly, for plants, the only candidates qualifying as potential TTL homologs are the tubulin tyrosine ligase-like 12 proteins. To get insight into the biological functions of these potential TTL homologs, we cloned the rice TTL-like 12 protein (OsTTLL12) and generated overexpression OsTTLL12-RFP lines in both rice and tobacco BY-2 cells. We found, unexpectedly, that overexpression of this OsTTLL12-RFP increased the relative abundance of detyrosinated α-tubulin in both coleoptile and seminal root, correlated with more stable microtubules. This was independent of the respective orientation of cortical microtubule, and followed by correspondingly changing growth of coleoptiles and seminal roots. A perturbed organization of phragmoplast microtubules and disoriented cell walls were further characteristics of this phenotype. Thus, the elevated tubulin detyrosination in consequence of OsTTLL12 overexpression affects structural and dynamic features of microtubules, followed by changes in the axiality of cell plate deposition and, consequently, plant growth.

Glycyrrhizin, the active compound of the TCM drug Gan Cao stimulates actin remodelling and defence in grapevine.

Actin remodelling by a membrane-associated oxidative process can sense perturbations of membrane integrity and activate defence. In the current work, we show that glycyrrhizin, a muscle relaxant used in Traditional Chinese Medicine, can activate oxidative burst and actin remodelling in tobacco BY-2 cells, which could be suppressed by diphenylene iodonium, an inhibitor of NADPH oxidases. Glycyrrhizin caused a dose-dependent delay of proliferation, and induced cell death, which was suppressed by addition of indole-acetic acid, a natural auxin that can mitigate RboH dependent actin remodelling. To test, whether the actin remodelling induced by glycyrrhizin was followed by activation of defence, several events of basal immunity were probed. We found that glycyrrhizin induced a transient extracellular alkalinisation, indicative of calcium influx. Furthermore, transcripts of phytoalexins genes, were activated in cells of the grapevine Vitis rupestris, and this induction was followed by accumulation of the glycosylated stilbene α-piceid. We also observed that glycyrrhizin was able to induce actin bundling in leaves of a transgenic grape, especially in guard cells. We discuss these data in frame of a model, where glycyrrhizin, through stimulation of RboH, can cause actin remodelling, followed by defence responses, such as calcium influx, induction of phytoalexins transcripts, and accumulation of stilbene glycosides.

A mitochondria-targeted coenzyme Q peptoid induces superoxide dismutase and alleviates salinity stress in plant cells.

Salinity is a serious challenge to global agriculture and threatens human food security. Plant cells can respond to salt stress either by activation of adaptive responses, or by programmed cell death. The mechanisms deciding the respective response are far from understood, but seem to depend on the degree, to which mitochondria can maintain oxidative homeostasis. Using plant PeptoQ, a Trojan Peptoid, as vehicle, it is possible to transport a coenzyme Q10 (CoQ10) derivative into plant mitochondria. We show that salinity stress in tobacco BY-2 cells (Nicotiana tabacum L. cv Bright Yellow-2) can be mitigated by pretreatment with plant PeptoQ with respect to numerous aspects including proliferation, expansion, redox homeostasis, and programmed cell death. We tested the salinity response for transcripts from nine salt-stress related-genes representing different adaptive responses. While most did not show any significant response, the salt response of the transcription factor NtNAC, probably involved in mitochondrial retrograde signaling, was significantly modulated by the plant PeptoQ. Most strikingly, transcripts for the mitochondrial, Mn-dependent Superoxide Dismutase were rapidly and drastically upregulated in presence of the peptoid, and this response was disappearing in presence of salt. The same pattern, albeit at lower amplitude, was seen for the sodium exporter SOS1. The findings are discussed by a model, where plant PeptoQ modulates retrograde signalling to the nucleus leading to a strong expression of mitochondrial SOD, what renders mitochondria more resilient to perturbations of oxidative balance, such that cells escape salt induced cell death and remain viable.

Hunting modulators of plant defence: the grapevine trunk disease fungus Eutypa lata secretes an amplifier for plant basal immunity.

Grapevine trunk diseases (GTDs) are progressively affecting vineyard longevity and productivity worldwide. To be able to understand and combat these diseases, we need a different concept of the signals exchanged between the grapevine and fungi than the well-studied pathogen-associated molecular pattern and effector concepts. We screened extracts from fungi associated with GTDs for their association with basal defence responses in suspension cells of grapevine. By activity-guided fractionation of the two selected extracts, O-methylmellein was identified as a candidate modulator of grapevine immunity. O-Methylmellein could not induce immune responses by itself (i.e. does not act as an elicitor), but could amplify some of the defence responses triggered by the bacterial elicitor flg22, such as the induction level of defence genes and actin remodelling. These findings show that Eutypa lata, exemplarily selected as an endophytic fungus linked with GTDs, can secrete compounds that act as amplifiers of basal immunity. Thus, in addition to elicitors that can trigger basal immunity, and effectors that down-modulate antibacterial basal immunity, once it had been activated, E. lata seems to secrete a third type of chemical signal that amplifies basal immunity and may play a role in the context of consortia of mutually competing microorganisms.